抄録
Ghrelin, isolated from the human and rat stomach, is the endogenous ligand for the growth hormone (GH) secretagogue-receptor (GHS-R). We previously reported that mRNAs for ghrelin and GHS-R as well as immunoreactive ghrelin were detected in the pancreatic islets. This study aimed to explore a physiological role of the islet ghrelin in the regulation of insulin release in rats and to elucidate its action mechanisms in β-cells. GHS-R blockade and anti-ghrelin antiserum markedly enhanced glucose-induced insulin release in isolated islets, while exogenously administered ghrelin suppressed it. In single β-cells, exogenous ghrelin attenuated glucose-induced first phase and oscillatory [Ca2+]i increases via interaction with GHS-R. Ghrelin also increased a tetraethylammonium-sensitive delayed outward K+ currents in single β-cells. These effects of endogenous and exogenous ghrelin were not observed in the islets and β-cells following treatment with pertussis toxin (PTX). These findings reveal that endogenous ghrelin in islets acts on β-cells to restrict glucose-induced insulin release via PTX-sensitive mechanisms. [Jpn J Physiol 55 Suppl:S80 (2005)]
